New York: A drug used to treat epilepsy may help reduce joint deformity associated with osteoarthritis, a study has revealed. Osteoarthritis, the most common form of arthritis, is a degenerative disease caused by the breakdown of the cartilage that reduces friction between joints. It usually occurs in the hands, hips and knees. Pain relief and lifestyle changes, such as exercise and losing excess weight, have long been the most commonly used therapies to treat joint stiffness and pain, but there is a great need for therapies that address the joint problems that occur in osteoarthritis. Can prevent breakage.
It is known that special proteins called sodium channels, found in cell membranes, generate electrical impulses in “excitable” cells within the muscles, nervous system and heart. In the new study, published in the journal Nature, the team found a special sodium channel called Nav1.7 in non-inflammatory cells, which produce collagen and help maintain joints in the body. A previous study by researchers at Yale University in the US had identified the important role of Nav1.7 in the transmission of pain signals.
In the new study, researchers removed the Nav1.7 gene from these collagen-producing cells and significantly reduced joint damage in two osteoarthritis models in mice. They also demonstrated that drugs used to block Nav1.7 – including carbamazepine, a sodium channel blocker currently used to treat epilepsy and trigeminal neuralgia – also reduced joint function in mice. Adequate protection is provided from damage.
“The function of sodium channels in non-excitable cells has been a mystery,” said Stephen G. Waxman, professor of neurology at Yale. “This new study provides a window into how small numbers of sodium channels can powerfully regulate the behavior of non-excitable cells.” “The findings open up new avenues for disease-preventing treatments,” said Wenyu Fu, a research scientist at the university.
